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Adenylate cyclase type 2 GABAA receptor Gamma- aminobutyric acid type B receptor N-type calcium channel G protein- activated inward rectifier potassium channel 1 Substance-P receptor Mu-type opioid receptor γ-Aminobutyric acid Substance P 3-Methylthiofentanyl cAMP Ca+ Ca+ Na+ Na+ γ-Aminobutyric acid 3-Methylthiofentanyl 3-Methylthiofentanyl ATP PPi GTP Pain Guanine nucleotide- binding protein G(i) subunit alpha-1 Magnesium Less GABA leads to disinhibition of dopamine cell firing in the spinal chord pain transmission neurons. This leads to less pain signalling and analgesia Decreased calcium levels lead to decreased neurotransmitter release. Less GABA is released for synaptic vesicles. 3-Methylthiofentanyl activates presynaptic mu opioid type receptors in the dorsal root ganglion The Gi subunit of the mu opioid receptor activates the inwardly rectifying potassium channel increasing K+ conductance. This causes membrane hyperpolarization decreasing the chances of neuronal firing/action potential. Post-Synaptic Neuron Pre-Synaptic Neuron Synapse Cytosol Synaptic Vesicle The mu opioid receptor through the gamma subunit inhibits voltage gated N-type calcium channels stopping the influx of calcium into the neuron. Methadone acts at A delta and C pain fibres in the dorsal horn of the spinal chord. By decreasing neurotransmitter action there is less pain transmittance into the spinal chord. This leads to less pain perception. C Pain Fibres The inhibition of adenylate cyclase prevents the production of cAMP which further prevents depolarization and pain signalling Substance P is also not released into the synapse which prevents the activation of pain signalling.
ADCY2 GABRG2 GABBR1 CACNA1B KCNJ3 TACR1 OPRM1 GNB1 GNG2 γ-Aminobutyric acid Substance P 3- Methylthiofentanyl cAMP Calcium Calcium Sodium Sodium γ-Aminobutyric acid 3- Methylthiofentanyl 3- Methylthiofentanyl Adenosine triphosphate Pyrophosphate Guanosine triphosphate Pain GNAI1
ADCY2 GABRG2 GABBR1 CACNA1B KCNJ3 TACR1 OPRM1 GNB1 GNG2